A fuller understanding of the effects of auditory tetanization in humans would inform better language and sensory learning paradigms; however, there are still unanswered questions. Here, we probe sustained changes in the event‐related potentials (ERPs) to 1020‐ and 980‐Hz tones following a rapid presentation of 1020‐Hz tone (every 75 ms, 13.3 Hz, tetanization). Consistent with some previous studies, we revealed the increase in the P2 ERP component after tetanization. Contrary to some other studies, we did not observe the expected N1 increase after tetanization even in the identical experimental sequence. We detected a significant N1 decrease after tetanization. Expanding previous research, we showed that P2 increase and N1 decrease are not specific to the stimulus type (tetanized 1020 Hz and non‐tetanized 980 Hz), suggesting the generalizability of tetanization effect to the not‐stimulated auditory tones, at least to those of the neighbouring frequency. The ERPs' tetanization effects were observed for at least 30 min—the most prolonged interval examined, consistent with the duration of long‐term potentiation, LTP. In addition, the tetanization effects were detectable in the blocks where the participants watched muted videos, an experimental setting that can be easily used in children and other challenging groups. Thus, auditory 13‐Hz stimulation affects brain processing of tones including those of neighbouring frequencies.
Independent Component Analysis (ICA) is a conventional approach to exclude non-brain signals such as eye movements and muscle artifacts from electroencephalography (EEG). A rejection of independent components (ICs) is usually performed in semiautomatic mode and requires experts’ involvement. As also revealed by our study, experts’ opinions about the nature of a component often disagree, highlighting the need to develop a robust and sustainable automatic system for EEG ICs classification. The current article presents a toolbox and crowdsourcing platform for Automatic Labeling of Independent Components in Electroencephalography (ALICE) available via link http://alice.adase.org/. The ALICE toolbox aims to build a sustainable algorithm to remove artifacts and find specific patterns in EEG signals using ICA decomposition based on accumulated experts’ knowledge. The difference from previous toolboxes is that the ALICE project will accumulate different benchmarks based on crowdsourced visual labeling of ICs collected from publicly available and in-house EEG recordings. The choice of labeling is based on the estimation of IC time-series, IC amplitude topography, and spectral power distribution. The platform allows supervised machine learning (ML) model training and re-training on available data subsamples for better performance in specific tasks (i.e., movement artifact detection in healthy or autistic children). Also, current research implements the novel strategy for consentient labeling of ICs by several experts. The provided baseline model could detect noisy IC and components related to the functional brain oscillations such as alpha and mu rhythm. The ALICE project implies the creation and constant replenishment of the IC database, which will improve ML algorithms for automatic labeling and extraction of non-brain signals from EEG. The toolbox and current dataset are open-source and freely available to the researcher community.
SHANK3 encodes a scaffold protein involved in postsynaptic receptor density in glutamatergic synapses, including those in the parvalbumin (PV)+ inhibitory neurons—the key players in the generation of sensory gamma oscillations, such as 40-Hz auditory steady-state response (ASSR). However, 40-Hz ASSR was not studied in relation to SHANK3 functioning. Here, we present a 15-year-old girl (SH01) with previously unreported duplication of the first seven exons of the SHANK3 gene (22q13.33). SH01’s electroencephalogram (EEG) during 40-Hz click trains of 500 ms duration binaurally presented with inter-trial intervals of 500–800 ms were compared with those from typically developing children (n = 32). SH01 was diagnosed with mild mental retardation and learning disabilities (F70.88), dysgraphia, dyslexia, and smaller vocabulary than typically developing (TD) peers. Her clinical phenotype resembled the phenotype of previously described patients with 22q13.33 microduplications (≈30 reported so far). SH01 had mild autistic symptoms but below the threshold for ASD diagnosis and microcephaly. No seizures or MRI abnormalities were reported. While SH01 had relatively preserved auditory event-related potential (ERP) with slightly attenuated P1, her 40-Hz ASSR was totally absent significantly deviating from TD’s ASSR. The absence of 40-Hz ASSR in patients with microduplication, which affected the SHANK3 gene, indicates deficient temporal resolution of the auditory system, which might underlie language problems and represent a neurophysiological biomarker of SHANK3 abnormalities.
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